The effect of cinnamic acid derivative on the activity of mitochondrial enzymes in brain tissue under conditions of experimental Parkinson's disease

Abstract

The aim: to evaluate the effect of cinnamic acid derivative on changes in mitochondrial enzymes activity in rats brain tissue under conditions of experimental Parkinson's disease. Materials and methods. Parkinson's disease was modeled in male Wistar rats by direct injection of rotenone solution (5 mg/ml) into the striatum. The analyzed compound 4-hydroxy-3,5-di-tretbutyl cinnamic acid and the reference ethylmethylhydroxypyridine succinate were administered orally in equivalent doses (100 mg/kg) for 30 days from the moment of pathology modeling. Next, a brain supernatant was obtained by differential centrifugation, in which changes in the activity of enzymes: citrate synthase, succinate dehydrogenase, cytochrome c oxidase and aconitase were evaluated. The obtained results were processed statistically. During the analysis, the StatPlus 7.0 application software package was used. Results. During the study, it was found that the administration of 4-hydroxy-3,5-di-tretbutyl cinnamic acid to rats increased the activity of citrate synthase, succinate dehydrogenase, cytochrome c oxidase and aconitase relative to untreated animals by 109.7% (p0.05); 53.6% (p0.05); 65.0% (p0.05) and 63.1% (p0.05), respectively, whereas against the background of the use of the reference, the activity of these enzymes increased by 56.3% (p0.05); 57.7% (p0.05); 71.7% (p0.05) and 49.1% (p0.05), respectively. At the same time, the activity of citrate synthase in animals treated by 4-hydroxy-3,5-di-tretbutyl cinnamic acid was higher than that in rats treated by the reference by 34.2% (p0.05). Conclusions. The study showed that the course administration of 4-hydroxy-3,5-di-tretbutyl cinnamic acid to animals with experimental Parkinson's disease is accompanied by an increase in the activity of mitochondrial enzymes, which may reflect the significant effect of this compound on the processes of mitochondrial biogenesis, mitophagy and generation of mitochondrial reactive oxygen species.